Jerusalem, 28 January, 2026 (TPS-IL) — A tiny experimental peptide developed by Israeli scientists may point to a new way of treating epilepsy, not only by reducing seizures but by slowing the disease’s progression and helping protect brain function, according to findings from a new preclinical study, Hebrew University of Jerusalem announced.
The research suggests that the compound, known as TXM-CB3, acts on biological processes that help epilepsy worsen over time. Unlike most existing treatments, which focus on suppressing seizures as they occur, the peptide targets oxidative stress and inflammation in the brain — two mechanisms increasingly linked to seizure recurrence, cognitive decline, and treatment resistance. The study also found that timing matters, with the strongest benefits seen when treatment begins early.
The findings were published in the peer-reviewed Redox Biology journal.
The World Health Organization estimates that around 50 million people live with epilepsy, making it one of the most common neurological disorders worldwide. It is characterized by recurrent, unprovoked seizures — sudden bursts of abnormal electrical activity in the brain. They can affect movement, sensation, awareness, behavior, and memory. There is no cure; treatments focus on controlling and reducing the seizures.
While anti-seizure medications can help many patients, up to 40 percent do not respond adequately, and current drugs generally do not prevent the condition from progressing.
“Our motivation was to look beyond seizure suppression,” said Prof. Tawfeeq Shekh-Ahmad of the Hebrew University’s School of Pharmacy and Faculty of Medicine. “Most epilepsy treatments focus on reducing seizures, but our goal was to see whether we could affect the underlying processes that may drive the disease forward.”
The study was led by PhD students Prince Kumar Singh and Shweta Maurya under Shekh-Ahmad’s supervision, in collaboration with Prof. Daphne Atlas of the Alexander Silberman Institute for Life Sciences. The researchers focused on TXM-CB3, a low-molecular-weight thioredoxin-mimetic peptide designed by Atlas. The compound is engineered to imitate thioredoxin, a naturally occurring protein that helps cells manage oxidative stress and regulate immune responses.
Disruptions in these protective systems are increasingly thought to play a central role in epilepsy, not only in triggering seizures but also in shaping how the disease evolves and becomes harder to treat over time. Previous work by Atlas showed that TXM-CB3 had protective effects in models of mild traumatic brain injury and inflammatory airway disease, prompting researchers to examine whether the same mechanisms could be relevant in epilepsy.
In laboratory experiments using nerve-cell models that produce seizure-like activity, the peptide reduced markers of oxidative damage and shifted immune signaling away from a strongly inflammatory state. These findings suggested that TXM-CB3 was acting on processes believed to sustain and amplify epileptic activity, rather than merely dampening electrical signaling in neurons.
The researchers then tested the compound in preclinical models designed to mimic severe, recurrent seizures seen in drug-resistant epilepsy. They examined two treatment windows with clear clinical relevance: early intervention shortly after a major seizure event, and later intervention after recurring seizures were already established.
When treatment was given early, seizures began later and occurred less frequently. Overall seizure burden was reduced, and brain regions critical for memory were better preserved. Animals treated early also showed behavioral improvements, including reduced anxiety-like behavior and better performance on short-term memory tasks.
When treatment began later, after epilepsy was already established, TXM-CB3 still reduced seizure activity over time. However, cognitive and memory impairments that had already developed did not significantly improve, highlighting a limited ability to reverse existing damage.
“The fact that we saw both reduced seizure activity and signs of brain protection in these experimental models strengthens the case for developing treatments that build on the body’s own protective pathways,” said Prof. Atlas.
In the near term, the findings from the TXM-CB3 study could inform the development of adjunct therapies for people with epilepsy, particularly those at high risk of recurring or drug-resistant seizures. By targeting oxidative stress and inflammation, the peptide — or similar compounds — could be used alongside standard anti-seizure medications to reduce seizure frequency and protect critical brain regions. Early intervention after an initial severe seizure may become a practical strategy, allowing clinicians to slow disease progression before cognitive or behavioral impairments develop.
Additionally, the peptide’s mechanism offers a potential option for patients who do not respond adequately to current treatments.
Over the longer term, TXM-CB3 and related compounds could help redefine epilepsy treatment from symptom management to disease modification. If clinical studies confirm the protective effects seen in preclinical models, therapies targeting the brain’s natural defense pathways could be used to preserve memory, reduce anxiety, and improve quality of life in addition to controlling seizures. Beyond epilepsy, the same strategy could inspire treatments for other neurological conditions driven by oxidative or inflammatory damage.
The researchers stress that the findings are based on experimental models and that further studies are needed to assess safety, dosing, and effectiveness in humans.
Related Topics
